Alcohol hangover effects on brain cortex non-synaptic mitochondria and synaptosomes bioenergetics
| Autor: | Silvia Lores-Arnaiz, Analía G. Karadayian, Paulina Lombardi, Juanita Bustamante |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
medicine.medical_specialty Health (social science) Oligomycin Bioenergetics Mitochondrion Toxicology medicine.disease_cause Biochemistry Binge Drinking Mice 03 medical and health sciences Behavioral Neuroscience Respirometry chemistry.chemical_compound 0302 clinical medicine Internal medicine Respiration medicine Animals Cerebral Cortex Membrane potential Synaptosome Ethanol Chemistry General Medicine Mitochondria 030227 psychiatry Endocrinology Neurology Energy Metabolism Alcoholic Intoxication 030217 neurology & neurosurgery Oxidative stress Synaptosomes |
| Zdroj: | Alcohol. 77:113-123 |
| ISSN: | 0741-8329 |
| DOI: | 10.1016/j.alcohol.2018.10.010 |
| Popis: | Alcohol hangover (AH) has been associated with oxidative stress and mitochondrial dysfunction. We herein postulate that AH-induced mitochondrial alterations can be due to a different pattern of response in synaptosomes and non-synaptic (NS) mitochondria. Mice received intraperitoneal (i.p.) injections of ethanol (3.8 g/kg) or saline and were sacrificed 6 h afterward. Brain cortex NS mitochondria and synaptosomes were isolated by Ficoll gradient. Oxygen consumption rates were measured in NS mitochondria and synaptosomes by high-resolution respirometry. Results showed that NS-synaptic mitochondria from AH animals presented a 26% decrease in malate-glutamate state 3 respiration, a 64% reduction in ATP content, 28–37% decrements in ATP production rates (malate-glutamate or succinate-dependent, respectively), and 44% inhibition in complex IV activity. No changes were observed in mitochondrial transmembrane potential (ΔΨ) or in UCP-2 expression in NS-mitochondria. Synaptosome respiration driving proton leak (in the presence of oligomycin), and spare respiratory capacity (percentage ratio between maximum and basal respiration) were 30% and 15% increased in hangover condition, respectively. Synaptosomal ATP content was 26% decreased, and ATP production rates were 40–55% decreased (malate-glutamate or succinate-dependent, respectively) in AH mice. In addition, a 24% decrease in ΔΨ and a 21% increase in UCP-2 protein expression were observed in synaptosomes from AH mice. Moreover, mitochondrial respiratory complexes I–III, II–III, and IV activities measured in synaptosomes from AH mice were decreased by 18%, 34%, and 50%, respectively. Results of this study reveal that alterations in bioenergetics status during AH could be mainly due to changes in mitochondrial function at the level of synapses. |
| Databáze: | OpenAIRE |
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